大鼠孕期甲氧滴滴涕暴露对子代成年雄鼠代谢综合征的影响
Effects of Prenatal Methoxychlor Exposure on Metabolic Syndrome in Adult Male Offspring Rats
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摘要:
目的 研究母鼠在孕中晚期暴露于甲氧滴滴涕(methoxychlor, MXC)后, 对其子代成年雄鼠发生代谢综合征的影响。 方法 孕鼠分为2 组:对照组和甲氧滴滴涕处理组。于孕期第11 天(gestational period 11, GD11)开始, 灌胃给药。将雄性仔鼠(每只母鼠保留2 只雄性仔鼠)正常饲养至成年(3 个月), 进行口服糖耐量实验(oral glucose tolerancetest, OGTT), 1 周后处死, 采集血清, 全自动生化分析仪检测血糖、总胆固醇及三酰甘油, 检测C 反应蛋白(C-reactiveprotein, CRP)、超氧化物歧化酶(superoxide dismutase, SOD)、丙二醛(malondialdehyde, MDA)、高密度脂蛋白(highdensity lipoprotein, HDL)及低密度脂蛋白(low density lipoprotein, LDL);ELISA试剂盒检测肿瘤坏死因子(tumor necrocisfactor-α, TNF-α)和脂联素。 结果 与对照组相比, MXC处理组仔鼠出生体重较低, 宫内生长迟缓(intrauterine growthretardation, IUGR)发生率增高(P<0.05, P<0.01)。其仔鼠在自然出生并正常饲料喂养下, 各时间段体重增长率与对照组比较, 差异无统计学意义。与对照组相比, MXC 处理组血糖曲线下面积(AUC)及各时间点血糖含量与正常对照组相比, 差异均无统计学意义。MXC 处理组的基础血糖、总胆固醇及三酰甘油与正常对照组相比, 差异均无统计学意义, 而高密度脂蛋白降低(P<0.01), 低密度脂蛋白升高(P<0.05), C-反应蛋白含量(CRP)升高(P<0.01), TNF-α 和MDA有升高趋势, 脂联素与SOD有降低的趋势。 结论 大鼠孕期甲氧滴滴涕暴露所致宫内发育迟缓的雄性仔鼠出生后, 在正常饲喂的情况下未出现“追赶性肥胖”, 成年后表现出代谢紊乱, 部分指标显示有代谢综合征的趋势。 Abstract:Objective To evaluate the effects of prenatal methoxychlor exposure in trimester of gestation on metabolic syndrome in adult male offspring rats. Methods Pregnant rats were allocated to a control group and a methoxychlor(MXC)group, and received intragastric administration starting from gestational day 11(GD11). Male offspring(2 retained of each maternal rats)were normally reared to adulthood(3 months after birth)and then were given an oral glucose tolerance test. After a week, the rats' fasting serum were collected to detect glucose, total cholesterol, and triglycerides by automatic biochemical analyzer; C-creative protein(CRP), superoxide dismutase(SOD), malondialdehyde(MDA), high density lipoprotein(HDL), and low density lipoprotein(LDL)by commercial kits; and tumor necrosis factor-α(TNF-α)and adiponectin by ELISA. Results Compared with the control group, lower pup birth weight and higher incidence of intrauterine growth retardation(IUGR)were found in the MXC group(P<0.05 and P<0.01, respectively), but no significant difference in the body weight growth rate was found. The MXC group showed no difference with the controls in blood glucose levels at each time spot and area under curve(AUC)of blood glucose. The offspring of the MXC group showed lower level of serum HDL than the control offspring(P<0.01), and for LDL, the results were reverse(P<0.05); while no difference was found in basic glucose, total cholesterol, and triglycerides between the two groups. The serum CRP of the MXC offspring was statistically higher than that of the control offspring(P<0.01), TNF-α and MDA were elevated but not significantly, and adiponectin and SOD were decreased but not significantly. Conclusion Prenatal methoxychlor exposure can not lead to catch-up growth in the adult male offspring rats with intrauterine growth retardation. Metabolic disorder is demonstrated in the development of male offspring rats, and some indicators suggest potential risk of metabolic syndrome.
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